Definitions of sepsis over the last 2 decades have changed multiple times as they relate to adult critical care. The definition of sepsis and sepsis syndromes in pediatric patients has been less well defined. The most recent published consensus definitions of sepsis in pediatric patients were published in 2005. These definitions were modeled after the adult definition and consensus guidelines published first in 1991 and then revised in 2001, 2008, 2012, and, most recently, 2016. The biggest change in adult consensus definitions occurred in the 2016 publication, which discarded systemic inflammatory response syndrome (SIRS) and severe sepsis; however, pediatric definitions continue to use these terms.
Based on the 2005 guidelines for pediatrics, SIRS requires both abnormal temperature and abnormal leukocyte count or 1 of those plus either tachypnea (> 2 standard deviations [SDs] above the mean for age) or abnormal heart rate (> 2 SDs above the mean for age or under the 10th percentile for age for those < 1 year old) without other explanation. Sepsis is defined as SIRS plus proven or suspected infection (bacteria, virus, fungus, or rickettsia). Severe sepsis is defined as sepsis plus dysfunction of at least 2 organs, acute respiratory distress syndrome, or cardiovascular dysfunction. Septic shock is sepsis plus cardiovascular dysfunction. The most recent adult definitions include sepsis, as defined previously with introduction of the use of sepsis-related organ failure assessment (SOFA) score, and septic shock requiring vasopressors despite appropriate fluid resuscitation and elevated lactate. It is likely that the definitions of pediatric sepsis will be reevaluated in light of the recent changes in adult practice.
PATHOGENESIS AND EPIDEMIOLOGY
The development of SIRS, sepsis, severe sepsis, and septic shock in the pediatric patient depends on a complex series of interrelated factors that include: host factors such as age, immunologic competence including vaccination status, comorbid conditions (including the presence of foreign material such as a central vascular, urinary, peritoneal, or intraventricular catheter), exposures (such as travel or day care), host response, site of entry of the infectious agent, and invading organism factors (including inoculum, virulence factors, and toxin production).
Central to the definition of sepsis is organ dysfunction as a result of infection. A variety of barriers, such as the skin and mucous membranes, serve as the first line that is breached at the beginning of the continuum of sepsis. After that breach, a series of events, first triggered by the innate immune response recognizing pathogen-associated molecular patterns (PAMPs) on the surface of invading organisms, starts the sepsis cascade by triggering release of cytokines and also awakening of the adaptive immune response, which is relatively slow because the adaptive immune response requires maturation and proliferation. This release triggers a systemic reaction to even a localized invasion, which ultimately results in loss of vascular integrity, apoptosis of immune cells, and reduced perfusion of vital organs. Clinically, this is evidenced by low blood pressure, cyanosis, delayed capillary refill, reduced urine output, and alterations in mental status.
Bacteremia may or may not be associated with a specific focus of infection. It may result from the extension of an infection originating elsewhere (eg, genitourinary, gastrointestinal, upper or lower respiratory tracts, or skin and soft tissue), or it may result in infection at other sites (eg, endocarditis, meningitis, facial cellulitis, osteomyelitis, pyelonephritis, or peritonitis). Recurrent or persistent bacteremia may result from established infectious foci (eg, endocarditis, abscess, or foreign body).
The epidemiology of pediatric sepsis is not well described globally and varies significantly between geographic regions in part ...